Laboratory Experimental Research in Biological Sciences, Federal University of Piaui, Piaui, Brazil.
Brain Res. 2010 Feb 22;1315:33-40. doi: 10.1016/j.brainres.2009.12.037. Epub 2009 Dec 23.
Recent researches have shown that antioxidant compounds may have certain neuroprotective effect against the neurotoxicity of seizures at cellular level. Ubiquinone (UQ), an antioxidant compound, exhibits a wide range of therapeutic effects that are attributed to its potent antioxidant capacity. The objective of the present study was to evaluate the neuroprotective effects of UQ in rats, against the observed oxidative stress during seizures induced by pilocarpine. Wistar rats were treated with either 0.9% saline (i.p., control group), UQ (5, 10 or 20 mg/kg, i.p., UQ5, UQ10 and UQ20 groups), pilocarpine (400 mg/kg, i.p., P400 group), or co-administration of pilocarpine with UQ group rats 30 min prior to UQ administration. After the treatments all groups were observed for 24 h. The antioxidant enzymatic activities as well as the hydroperoxide concentrations were measured using spectrophotometric methods and the results were analyzed. In pilocarpine group there was a significant increase in hydroperoxides concentration and glutathione peroxidase activity. However, no alteration was observed in superoxide dismutase and catalase activities. Antioxidant treatment significantly reduced the hydroperoxide content and increased the superoxide dismutase, catalase and glutathione peroxidase activities in rat hippocampus during seizures induced by pilocarpine. Our findings strongly support the hypothesis that oxidative stress in hippocampus occurs during seizures induced by pilocarpine, which indicates that brain damage induced by the oxidative process plays a crucial role in seizures pathogenic consequences. Our result also suggests that ubiquinone can exert significant neuroprotective effects that might be useful in the treatment of neurodegenerative diseases.
最近的研究表明，抗氧化化合物可能对细胞水平的癫痫毒性具有一定的神经保护作用。抗氧化化合物泛醌 (UQ) 表现出广泛的治疗作用，这归因于其强大的抗氧化能力。本研究的目的是评估 UQ 对大鼠的神经保护作用，以对抗匹鲁卡品诱导的癫痫发作期间观察到的氧化应激。Wistar 大鼠分别用 0.9%生理盐水 (i.p.，对照组)、UQ (5、10 或 20 mg/kg，i.p.，UQ5、UQ10 和 UQ20 组)、匹鲁卡品 (400 mg/kg，i.p.，P400 组) 或匹鲁卡品与 UQ 组大鼠共同给药治疗，UQ 给药前 30 分钟。所有组治疗后均观察 24 小时。使用分光光度法测量抗氧化酶活性和过氧化物浓度，并分析结果。在匹鲁卡品组中，过氧化物浓度和谷胱甘肽过氧化物酶活性显著增加。然而，超氧化物歧化酶和过氧化氢酶活性没有改变。抗氧化治疗在匹鲁卡品诱导的癫痫发作期间显著降低了大鼠海马中的过氧化物含量，并增加了超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶的活性。我们的研究结果强烈支持这样一种假设，即在匹鲁卡品诱导的癫痫发作期间，海马中发生氧化应激，这表明氧化过程引起的脑损伤在癫痫发病后果中起着至关重要的作用。我们的结果还表明，泛醌可以发挥显著的神经保护作用，这可能对治疗神经退行性疾病有用。
